Cerebrospinal fluid β‐amyloid and phospho‐tau biomarker interactions affecting brain structure in preclinical Alzheimer disease

脑脊液 生物标志物 萎缩 病理 磁共振成像 神经影像学 阿尔茨海默病 τ蛋白 病态的 腰椎穿刺 医学 内科学 疾病 心理学 神经科学 化学 放射科 生物化学
作者
Juan Fortea,Eduard Vilaplana,Daniel Alcolea,María Carmona‐Iragui,María Belén Sánchez‐Saudinós,Isabel Sala,Sofía Antón‐Aguirre,Sofía González,Santiago López de Medrano,Jordi Pegueroles,Estrella Morenas,Jordi Clarimón,Rafael Blesa,Alberto Lleó
出处
期刊:Annals of Neurology [Wiley]
卷期号:76 (2): 223-230 被引量:110
标识
DOI:10.1002/ana.24186
摘要

To assess the relationships between core cerebrospinal fluid (CSF) biomarkers and cortical thickness (CTh) in preclinical Alzheimer disease (AD).In this cross-sectional study, normal controls (n = 145) from the Alzheimer's Disease Neuroimaging Initiative underwent structural 3T magnetic resonance imaging (MRI) and lumbar puncture. CSF β-amyloid1-42 (Aβ) and phospho-tau₁₈₁p (p-tau) levels were measured by Luminex assays. Samples were dichotomized using published cutoffs (Aβ(+) /Aβ(-) and p-tau(+) /ptau(-)). CTh was measured by Freesurfer. CTh difference maps were derived from interaction and correlation analyses. Clusters from the interaction analysis were isolated to analyze the directionality of the interaction by analysis of covariance.We found a significant biomarker interaction between CSF Aβ and CSF p-tau levels affecting brain structure. Cortical atrophy only occurs in subjects with both Aβ(+) and p-tau(+). The stratified correlation analyses showed that the relationship between p-tau and CTh is modified by Aβ status and the relationship between Aβ and CTh is modified by p-tau status. p-Tau-dependent thinning was found in different cortical regions in Aβ(+) subjects but not in Aβ(-) subjects. Cortical thickening was related to decreasing CSF Aβ values in the absence of abnormal p-tau, but no correlations were found in p-tau(+) subjects.Our data suggest that interactions between biomarkers in AD result in a 2-phase phenomenon of pathological cortical thickening associated with low CSF Aβ, followed by atrophy once CSF p-tau becomes abnormal. These interactions should be considered in clinical trials in preclinical AD, both when selecting patients and when using MRI as a surrogate marker of efficacy.
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